Zebrafish Beyond the Bench: The 'Plataforma Zebrafish Open Doors' Programme.

The Butantan Institute is a pioneering Brazilian health sciences institution, which also houses a large science park with museums that contribute to ongoing science education for schools and the wider community. In recent years, as part of Butantan Institute's Plataforma Zebrafish™, zebrafish embryos have been used for the dissemination of scientific knowledge during on-site events and as part of outreach campaigns to non-scientific audiences, mostly children. The aim of this work is mainly to demystify the activities of the scientific researcher, highlight the role of science in the furthering of knowledge, and increase public interest and confidence in science. In this article, the Institute's 'Plataforma Zebrafish Open Doors' programme is described, which offered guided tours of the laboratory facilities. The tours gave visitors the opportunity to observe zebrafish research and embryo development, and to use the knowledge gained from this experience as a framework for understanding fundamental ethical issues. During the 2-day event, around 800 visitors (most of them school-age children) attended. Together with the guided tours, our experience of outreach offered meaningful opportunities to bring children and members of the public closer to science and 'real-life' scientists, hopefully inspiring and encouraging the next generation of scientists. It also gave the scientists an opportunity to engage more closely with wider society. We believe that these activities also substantially contribute to the wider dissemination of relevant experimental results that have been obtained with public funding and that impact society in general.

Knockdown of miR-26a in zebrafish leads to impairment of the anti-inflammatory function of TnP in the control of neutrophilia.

Our recent data show the valuable potential of TnP for the development of a new and safe anti-inflammatory drug due to its ability to control the traffic and activation of leukocytes in response to inflammation. Although there is considerable knowledge surrounding the cellular mechanisms of TnP, less is known about the mechanistic molecular role of TnP underlying its immunomodulatory functions. Here, we conducted investigations to identify whether miRNAs could be one of the molecular bases of the therapeutic effect of TnP. Using a zebrafish model of neutrophilic inflammation with a combination of genetic gain- and loss-of-function approaches, we showed that TnP treatment was followed by up-regulation of only four known miRNAs, and mature dre-miR-26a-1, herein referred just as miR-26a was the first most highly expressed. The knockdown of miR-26a ubiquitously resulted in a significant reduction of miR-26a in embryos, accompanied by impaired TnP immunomodulatory function observed by the loss of the control of the removal of neutrophils in response to inflammation, while the overexpression increased the inhibition of neutrophilic inflammation promoted by TnP. The striking importance of miR-26a was confirmed when rescue strategies were used (morpholino and mimic combination). Our results identified miR-26a as an essential molecular regulator of the therapeutic action of TnP, and suggest that miR-26a or its targets could be used as promising therapeutic candidates for enhancing the resolution of inflammation.